网格蛋白介导内吞作用中的力产生的分子机制。
Molecular mechanisms of force production in clathrin-mediated endocytosis.
机构信息
Department of Molecular Biophysics and Biochemistry, Yale University, New Haven, CT, USA.
Nanobiology Institute, Yale University, West Haven, CT, USA.
出版信息
FEBS Lett. 2018 Nov;592(21):3586-3605. doi: 10.1002/1873-3468.13192. Epub 2018 Jul 28.
Abstract
During clathrin-mediated endocytosis (CME), a flat patch of membrane is invaginated and pinched off to release a vesicle into the cytoplasm. In yeast CME, over 60 proteins-including a dynamic actin meshwork-self-assemble to deform the plasma membrane. Several models have been proposed for how actin and other molecules produce the forces necessary to overcome the mechanical barriers of membrane tension and turgor pressure, but the precise mechanisms and a full picture of their interplay are still not clear. In this review, we discuss the evidence for these force production models from a quantitative perspective and propose future directions for experimental and theoretical work that could clarify their various contributions.
摘要
在网格蛋白介导的胞吞作用（CME）中，细胞膜的一个扁平斑块向内凹陷并被切断，从而将囊泡释放到细胞质中。在酵母 CME 中，超过 60 种蛋白质——包括动态肌动蛋白网格——自组装以改变质膜的形状。已经提出了几种模型来解释肌动蛋白和其他分子如何产生克服膜张力和膨压机械障碍所需的力，但这些机制的确切机制及其相互作用的全貌仍然不清楚。在这篇综述中，我们从定量的角度讨论了这些力产生模型的证据，并提出了未来进行实验和理论工作的方向，这可能会澄清它们的各种贡献。
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